Tiotropium/Olodaterol Reduce Cigarette Smoking Extract-induced Cell Death in BEAS-2B Bronchial Epithelial Cells
Background: COPD is characterized by progressive irreversible airflow limitation. Cigarette smoking is an important risk factor for destruction of lung parenchyma or emphysema. Disruption of epithelial layer integrity may contribute to lung injury in response to CS exposure. Tiotropium/Olodaterol act as bronchodilator to treatment COPD by preventing ASM contraction and muscle relaxation; however, the effect of dual bronchodilator on epithelial cell injury and its underlying mechanism is still
... echanism is still unclear. Methods: In this study, we aim to evaluate the effect of Tiotropium/Olodaterol on CSE-mediate cell death, with a special focus on autophagy. In this study, we investigated the effects of Tiotropium/Olodaterol on cell viability, the mitochondrial membrane potential (MMP; Δφm), and autophagy in BEAS-2B bronchial epithelial cells. Results: Tiotropium/olodaterol significantly inhibit CSE-induce cell death, mitochondria dysfunction and autophagy in response to short-term treatment with CSE. Moreover, decrease in ERK and JNK activation after CSE treatment were reversed by Tiotropium/olodaterol treatment. Conclusions: Tiotropium/olodaterol have protective effect against CSE-induced cell death which may related to induction of autophagy via activating ERK and JNK. In this study, we provide a possible novel mechanism for dual-bronchodilator in COPD treatment.